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OBJECTIVE: To investigate abdominal aortic aneurysm (AAA) screening rates in the 6 months before and after the introduction of updated Canadian Task Force on Preventive Health Care (CTFPHC) guidelines to determine effects on practice patterns, as well as to determine whether certain patient characteristics impact AAA screening rates. DESIGN: Retrospective chart review. SETTING: Academic family health centre in London, Ont. PARTICIPANTS: Male patients between the ages of 65 and 80. MAIN OUTCOME MEASURES: Screening rates for AAA before and after the guideline update were compared using the normal approximation of the binomial distribution. Analysis of demographic characteristic effects on screening rates was completed with the Fisher exact test. Number of visits to the clinic with a primary care provider within the study period and imaging type were collected. RESULTS: Of the 266 patients included in the study, 160 patients were eligible for screening at the start of the study period, 6 months before publication of the CTFPHC AAA guideline. Individuals eligible for screening visited the clinic an average (SD) of 2.44 (1.82) times in the 6 months before and 2.66 (1.99) times in the 6 months after. Overall, 69 individuals had AAA screening completed and 9 had a discussion of AAA screening without any imaging, for a total uptake rate of 88.5% for those who had screening recommended. The overall imaging rate was 48.9%. There was no statistically significant difference in screening rates between the time periods (P=.337) among those eligible for screening. For demographic characteristics for risk stratification, 7 individuals had a documented family history, of whom 5 had imaging of their abdominal aorta performed, plus 1 additional individual who had screening recommended but not completed. This was not statistically significant relative to the total population (P=.0598). Positive smoking status (active or ex-smoker) was more common, with 135 individuals having a relevant smoking history. Approximately half of these current and former smokers (68 individuals [50.4%]) had any sort of abdominal aortic imaging performed or recommended, which was not statistically significantly different compared with non-smokers (62 of 126 imaging performed or recommended, 49.2%; P=.9016). CONCLUSION: Screening practices did not change appreciably with the introduction of the CTFPHC AAA screening guidelines. Further research is needed to improve AAA screening rates. It is worth exploring electronic medical record–based reminders, nursing staff involvement in screening, screening programs via public health, and point-of-care ultrasound screening in a primary care setting.

Background Computerized algorithms known as symptom checkers aim to help patients decide what to do should they have a new medical concern. However, despite widespread implementation, most studies on symptom checkers have involved simulated patients. Only limited evidence currently exists about symptom checker safety or accuracy when used by real patients. We developed a new prototype symptom checker and assessed its safety and accuracy in a prospective cohort of patients presenting to primary care and emergency departments with new medical concerns. Method A prospective cohort study was done to assess the prototype’s performance. The cohort consisted of adult patients (≥16 years old) who presented to hospital emergency departments and family physician clinics. Primary outcomes were safety and accuracy of triage recommendations to seek hospital care, seek primary care, or manage symptoms at home. Results Data from 281 hospital patients and 300 clinic patients were collected and analyzed. Sensitivity to emergencies was 100% (10/10 encounters). Sensitivity to urgencies was 90% (73/81) and 97% (34/35) for hospital and primary care patients, respectively. The prototype was significantly more accurate than patients at triage (73% versus 58%, p Interpretation The prototype symptom checker was superior to patients in deciding the most appropriate treatment setting for medical issues. This symptom checker could reduce a significant number of unnecessary hospital visits, with accuracy and safety outcomes comparable to existing data on telephone triage.

Streptococcus pyogenes is a globally prominent bacterial pathogen that exhibits strict tropism for the human host, yet bacterial factors responsible for the ability of S. pyogenes to compete within this limited biological niche are not well understood. Using an engineered recombinase-based in vivo expression technology (RIVET) system, we identified an in vivo-induced promoter region upstream of a predicted Class IIb bacteriocin system in the M18 serotype S. pyogenes strain MGAS8232. This promoter element was not active under in vitro laboratory conditions, but was highly induced within the mouse nasopharynx. Recombinant expression of the predicted mature S. pyogenes bacteriocin peptides (designated SpbM and SpbN) revealed that both peptides were required for antimicrobial activity. Using a gain of function experiment in Lactococcus lactis, we further demonstrated S. pyogenes immunity function is encoded downstream of spbN. These data highlight the importance of bacterial gene regulation within appropriate environments to help understand mechanisms of niche adaptation by bacterial pathogens.

Streptococcus pyogenes is a globally prominent human-specific pathogen that is responsible for an enormous burden of infectious disease. Despite intensive experimental efforts to understand the molecular correlates that contribute to invasive infections, there has been less focus on S. pyogenes carriage and local infection of the nasopharynx. This chapter describes an acute nasopharyngeal infection model in mice that is utilized in our laboratory to study the role of superantigen toxins in the biology of S. pyogenes. We also describe a method to detect superantigen-specific T cell activation in vivo.

Streptococcus pyogenes is a globally prominent human-specific pathogen that is responsible for an enormous burden of infectious disease. Despite intensive experimental efforts to understand the molecular correlates that contribute to invasive infections, there has been less focus on S. pyogenes carriage and local infection of the nasopharynx. This chapter describes an acute nasopharyngeal infection model in mice that is utilized in our laboratory to study the role of superantigen toxins in the biology of S. pyogenes. We also describe a method to detect superantigen-specific T cell activation in vivo.

Introduction: Cellulosimicrobium cellulans is a rare human pathogen that is associated with chronic immunosuppression, such as human immunodeficiency virus infection, post‐transplantation or end‐stage renal disease. Case presentation: A 59‐year old man with a past medical history of significant cardiovascular, cerebrovascular and peripheral vascular disease was admitted to the intensive care unit (ICU) with intractable seizures. Physical examination, radiographic imaging and culture results suggested the patient had developed metabolic encephalopathy due to pneumonia caused by Staphylococcus aureus and Moraxella catarrhalis. The patient recovered neurologically with the use of broad‐spectrum antibiotics but developed acute renal failure during his stay. Seven days later, he relapsed into seizure activity and two separate blood cultures grew Cellulosimicrobium cellulans. Despite maximal antibiotic therapy, the patient continued to deteriorate. After 16 days, the patient’s family withdrew care and he subsequently died. Conclusion: We report the isolation of Cellulosimicrobium cellulans from a patient who developed acute renal failure following a prolonged stay in the ICU for sepsis encephalopathy.

Establishing the genetic determinants of niche adaptation by microbial pathogens to specific hosts is important for the management and control of infectious disease. Streptococcus pyogenes is a globally prominent human-specific bacterial pathogen that secretes superantigens (SAgs) as ‘trademark’ virulence factors. SAgs function to force the activation of T lymphocytes through direct binding to lateral surfaces of T cell receptors and class II major histocompatibility complex (MHC-II) molecules. S. pyogenes invariably encodes multiple SAgs, often within putative mobile genetic elements, and although SAgs are documented virulence factors for diseases such as scarlet fever and the streptococcal toxic shock syndrome (STSS), how these exotoxins contribute to the fitness and evolution of S. pyogenes is unknown. Here we show that acute infection in the nasopharynx is dependent upon both bacterial SAgs and host MHC-II molecules. S. pyogenes was rapidly cleared from the nasal cavity of wild-type C57BL/6 (B6) mice, whereas infection was enhanced up to ∼10,000-fold in B6 mice that express human MHC-II. This phenotype required the SpeA superantigen, and vaccination with an MHC –II binding mutant toxoid of SpeA dramatically inhibited infection. Our findings indicate that streptococcal SAgs are critical for the establishment of nasopharyngeal infection, thus providing an explanation as to why S. pyogenes produces these potent toxins. This work also highlights that SAg redundancy exists to avoid host anti-SAg humoral immune responses and to potentially overcome host MHC-II polymorphisms., Author Summary Streptococcus pyogenes is the most common cause of bacterial pharyngitis, also known as ‘strep throat’. However, this organism is also responsible for a range of other important human illnesses including necrotizing fasciitis and rheumatic heart disease (RHD). Indeed, complications from RHD and invasive infections by S. pyogenes are responsible for over one half million deaths per year in the world. S. pyogenes produces potent toxins called superantigens (SAgs), also known as the scarlet fever or erythrogenic toxins. SAgs have been studied for many years, yet we don't understand what purpose SAgs play in the life cycle of S. pyogenes. Rather than studying SAgs in the context of serious streptococcal disease, we studied the role of SAgs in a nasopharyngeal infection model. Our work demonstrates that for S. pyogenes to efficiently infect mice, the mice must express a human protein that is a receptor for the SAgs, and that S. pyogenes must produce SAgs. We further show that immunizing against SAgs prevents nasopharyngeal infection. This work demonstrates that SAgs are important factors for establishing infection by S. pyogenes and that SAgs may be potential candidates for inclusion within a S. pyogenes vaccine.